Mesenchymal stem cells use extracellular vesicles to outsource mitophagy and shuttle microRNAs

Nat Commun. 2015 Oct 7:6:8472. doi: 10.1038/ncomms9472.

Abstract

Mesenchymal stem cells (MSCs) and macrophages are fundamental components of the stem cell niche and function coordinately to regulate haematopoietic stem cell self-renewal and mobilization. Recent studies indicate that mitophagy and healthy mitochondrial function are critical to the survival of stem cells, but how these processes are regulated in MSCs is unknown. Here we show that MSCs manage intracellular oxidative stress by targeting depolarized mitochondria to the plasma membrane via arrestin domain-containing protein 1-mediated microvesicles. The vesicles are then engulfed and re-utilized via a process involving fusion by macrophages, resulting in enhanced bioenergetics. Furthermore, we show that MSCs simultaneously shed micro RNA-containing exosomes that inhibit macrophage activation by suppressing Toll-like receptor signalling, thereby de-sensitizing macrophages to the ingested mitochondria. Collectively, these studies mechanistically link mitophagy and MSC survival with macrophage function, thereby providing a physiologically relevant context for the innate immunomodulatory activity of MSCs.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Arrestins / metabolism
  • Blotting, Western
  • Cell-Derived Microparticles / metabolism
  • Exosomes / metabolism
  • Extracellular Vesicles / metabolism*
  • Extracellular Vesicles / ultrastructure
  • Flow Cytometry
  • Humans
  • Macrophages / metabolism*
  • Mesenchymal Stem Cells / metabolism*
  • Mesenchymal Stem Cells / ultrastructure
  • Mice
  • MicroRNAs / metabolism*
  • Microscopy, Electron
  • Mitochondria / metabolism*
  • Mitophagy / physiology*
  • Myeloid Differentiation Factor 88 / genetics
  • Oxidative Stress
  • Receptors, Immunologic / genetics
  • Signal Transduction
  • Silicosis / metabolism*
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 9 / genetics
  • Toll-Like Receptors / metabolism

Substances

  • Arrestins
  • Marco protein, mouse
  • MicroRNAs
  • Myd88 protein, mouse
  • Myeloid Differentiation Factor 88
  • Receptors, Immunologic
  • Tlr4 protein, mouse
  • Tlr9 protein, mouse
  • Toll-Like Receptor 4
  • Toll-Like Receptor 9
  • Toll-Like Receptors

Associated data

  • GEO/GSE71241